This animal study examined subchronic exposure to a 30 mT static magnetic field for 10 weeks in young and 36-month-old rats (n=27). The abstract reports decreased lymphocyte counts and increased NLR in both age groups, with PLR increases limited to young rats and platelet decreases reported in older rats. The authors interpret the findings as age-dependent immune/inflammation modulation, framing potential proinflammatory risk in younger animals and immunosuppressive/stress-related effects in older animals.

This RF Safe article argues that pulsed, low-frequency-modulated wireless radiofrequency exposures could disrupt voltage-gated ion channel timing (via the S4 voltage sensor), leading to altered immune-cell signaling, mitochondrial oxidative stress, and downstream innate immune activation and inflammation. It presents a mechanistic narrative linking small membrane-potential shifts to changes in calcium and proton channel behavior, then to mitochondrial reactive oxygen species and inflammatory pathways (e.g., cGAS–STING, TLR9, NLRP3). The post cites animal findings and a described 2025 mouse gene-expression study as supportive, but the piece itself is not a peer-reviewed study and some claims are presented as deterministic without providing full methodological details in the excerpt.

This RF Safe article argues that persistent low-intensity, pulsed RF exposure could disrupt the timing of voltage-gated ion channel activity by affecting the S4 voltage-sensing region, leading to downstream changes in calcium/proton signaling, mitochondrial stress, and immune dysregulation. It proposes a mechanistic chain from altered ion gating to increased mitochondrial ROS, mitochondrial DNA release, and activation of innate immune pathways (e.g., cGAS-STING, TLR9, NLRP3). The post cites “multiple reviews and experiments” and references animal findings and a 2025 mouse study, but the provided text does not include enough study details to independently assess the strength of the evidence.

An RF Safe article argues that plasma membrane potential (Vm) is a key control variable for immune cell behavior by shaping ion driving forces, especially Ca2+ influx through CRAC channels and K+ channel–mediated hyperpolarization. It describes proposed links between Vm-regulated ion flux and downstream immune functions such as T-cell activation (NFAT/NF-κB signaling), macrophage polarization, respiratory burst capacity, and NLRP3 inflammasome activation. The piece also mentions that external electric fields can influence T-cell migration and activation markers under some conditions, but it does not present new experimental data in the excerpt provided.